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Furman University

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Narrative Documents

6-2-2015

The History of Autism


Kieran A. Cook

Alissa N. Willmerdinger

Follow this and additional works at: http://scholarexchange.furman.edu/schopler-about


Part of the Psychology Commons

Recommended Citation
Cook, Kieran A. and Willmerdinger, Alissa N., "The History of Autism" (2015). Narrative Documents. Book 1.
http://scholarexchange.furman.edu/schopler-about/1

This Narrative Document is made available online by part of the Furman University Scholar Exchange (FUSE). It has been accepted for inclusion in
Narrative Documents by an authorized FUSE administrator. For terms of use, please refer to the FUSE Institutional Repository Guidelines. For more
information, please contact scholarexchange@furman.edu.
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The History of Autism

Since the first description of autistic tendencies in the early 1800s, the definition and

diagnostic criteria for autism have changed radically. The first Diagnostic Statistical Manual

(DSM) categorized autism as a childhood subtype of schizophrenia (American Psychiatric

Association, 1952) though autism was eventually separated from schizophrenia, becoming its

own diagnosis. Over time autism evolved into a diagnostic spectrum by the time the DSM-5 was

published in 2013. Autism is becoming more prevalent, and the diagnostic criteria and definition

are likely to continue to change in the future.

Early Conceptualizations of Autism

In 1798 before the first use of the word autism, French physician Jean-Marc Gaspard

Itard described Victor the Wild Boy of Aveyron, a young boy who was found after being isolated

in the woods for 11 years, as being socially withdrawn in addition to having language and

intellectual disabilities. He recognized Victor as being developmentally different from other

children his age. Itard’s description of Victor’s tendencies would later be formally characterized

as autistic (Itard, 1932).

Over a hundred years later, in 1910, Paul Eugen Bleuler, a Swiss psychiatrist, used the

word ‘autism’ for the first time when describing specific symptoms of schizophrenic patients

where they became withdrawn from others (Greydanus & Toledo-Pereyra, 2012). Later in 1927,

a student of Bleuler, Eugene Minkowski, described autism as the “trouble generator” of

schizophrenia (Minkowski, 2001).

Shifting Perspectives on the Origins of Autism.


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Psychogenic perspectives of autism

In the early 20th century, the predominant theories on autism adopted a psychogenic

approach, according to which autism is caused by emotional or psychological factors rather than

ones that are biological or physical. Some of this was grounded in Freudian psychoanalytic

theory, which was popular at the time. These psychogenic explanations for autism were widely

accepted among the medical field and persisted due to a lack of medical research investigating

the cause of autism.

Researchers who were proponents of the psychogenic approach focused specifically on

parenting styles as the underlying cause of autistic behaviors in children. In the 1940s, Kanner

described autism as the “children’s inability to relate themselves in the ordinary way to people

and situations from the beginning of life,” and separated autism from a subtype of schizophrenia

into its own category as “infantile autism” (Kanner, 1943). Kanner continued to describe autism

as “an extreme autistic aloneness that, whenever possible, disregards, ignores, shuts out anything

that comes to the child from the outside” (Kanner, 1943). One of the most interesting aspects of

Kanner’s view of autism was his theory of “refrigerator mothers,” which states the cause of

autism as “lack of maternal warmth.” Though Kanner believed in some innate properties, this

would be his main argument for the cause of autism (Kanner, 1943).

After Kanner’s separation of infantile autism and childhood type schizophrenia, Hans

Asperger, a German pediatrician, identified a milder form of autism. In 1944 he highlighted this

milder form of autism in his study of boys all of higher intelligence who suffered from trouble

with social interaction and obsessive interests (Asperger & Frith, 1991).

Following Asperger in the 1950s, the “refrigerator mothers” theory was popularized by

childhood psychologist, Bruno Bettelheim, through his use of the media to perpetuate the idea
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that parents were the cause of autism (History of Autism, 2010). Bettelheim’s further blame of

parents for causing autism resulted in the psychogenic perspective creating a range of therapeutic

approaches. Most notable was Bettelheim’s approach that included removing children from the

negative influence of their parents to live in residential treatment facilities (Mesibov, Shea, &

Schopler, 2005). He compared parents of autistic children to concentration camp guards and

their children to prisoners and victims saying, “emotionally cold parents had produced the

autistic features in their children through unconscious feelings of hostility and rejection.”

Children were even encouraged to play on a large stone sculpture of a woman to learn that their

mother had a “heart cold as stone” (Mesibov, Shea, & Schopler, 2005).

A shift toward biological explanations of autism

The idea that parents were the cause of autism was controversial. Beginning in the

1960s, a different approach to autism research began to take shape. Instead of focusing solely on

psychogenic and emotional causes of autism, researchers began to shift their focus toward

understanding the biological and behavioral mechanisms of autism. Early biological research

started with Stella Chess in the 1960s and her research of autism as a neurological disease

(Pearce, 2007).

In 1964, Bernard Rimland founded the Autism Society of America. Rimland was also a

proponent in refuting Bettelheim’s ‘refrigerator mother’ theory; instead extending the theory that

autism had a biological basis. In his book, Infantile autism: The syndrome and its implications

for a neural theory of behavior, Rimland disproved the “refrigerator mothers” theory and

proposed that there was a genetic component responsible for autism (Edelson, 2014).

Research examining biological and physical underpinnings of autism has not been

without its share of controversy. The Lancet published an article in 1998 by Wakefield, Murch,
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Anthony, Linnell, Casson, et al., which suggested that the Measles, Mumps and Rubella (MMR)

vaccine was causing autism (Rao, 2011; Wakefield et al., 1998). This article argued that the

preservative thimerosal in the vaccine was an underlying cause. Subsequent studies by the FDA

and CDC found no evidence for the claim; however, in response to the article the preservative

thimerosal was removed from vaccines in 1999 (Thimerosal in Vaccines, 2014). Furthermore,

any existing vaccines that contained thimerosal expired in 2003 (Thimerosal in Vaccines, 2014).

The Lancet article was finally retracted in 2010 after being exposed as fraudulent (Rao, 2011).

To date there is no credible evidence that vaccines are a cause of autism.

Alongside a shift in focus away from psychogenic origins and toward biological origins,

there was also a movement to focus on the treatment of autistic behaviors. This was guided by

behaviorist principles, which were popularized in 1965 by Ole Ivar Lovaas, who developed

Applied Behavior Analysis (ABA) therapy (Lovaas Institute, 2005). In ABA therapy “the

overall goal is to break down skills into manageable pieces and then build upon those skills so

that a child learns how to learn in a natural environment” (Lovaas Institute, 2005).

In 1972, Eric Schopler started another intervention program, the Treatment and

Education of Autistic and Related Communication Handicapped Children (TEACCH) program

at UNC Chapel Hill, a program that continues to this day. This program provides intervention,

training, and other programs for individuals with autism, and uses parents as “co-therapists” to

help treat autistic children (Mesibov et al., 2005). For more information about the TEACCH

program visit the section of this FUSE page entitled “TEACCH Research.”

Summary of the Changing Definitions of Autism


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The definition of autism and the diagnostic criteria for autism have changed several times

in the last hundred years. Autism was initially listed as a form of childhood schizophrenia in the

DSM-I (American Psychiatric Association, 1952) and under this diagnostic criteria, the first

epidemiological study was conducted in 1966 and found that 4.5/10,000 children had autism

(Lotter, 1967), suggesting that it was a rare disorder. Autism was not officially separated from

schizophrenia until 1980 when it was labeled infantile autism in the DSM-III and 6 main

criterions were necessary for diagnosis (Gernsbacher, Dawson, & Goldsmith, 2005). In 1987,

another revision occurred to the definition and diagnostic criteria and the “infantile autism”

definition expanded to become “autism spectrum disorder” in the DSM-III-R (American

Psychiatric Association, 1987). The clinical definition of autism changed yet again in 1994

when Pervasive Developmental Disorder-Not Otherwise Specified & Asperger’s syndrome were

added to the DSM-IV through the expansion of the diagnostic criteria to include subtypes of

autism (Baker, 2013). Another epidemiological study conducted by the Centers for Disease

Control in 2009 estimated that 1 in 110 children have autism spectrum disorder, which was an

increase from the 1 in 150 estimate calculated in 2007 (Baio, 2012). The CDC notes that

prevalence rates increased partially from improved screening and diagnostic techniques. Finally,

in 2013, the DSM-5 was published which again changed the definition of autism by

consolidating the five subcategories of autism spectrum disorder (ASD) into one umbrella

diagnosis of ASD with Asperger’s no longer being a separate condition. Autism Spectrum

Disorder is now defined by two categories: impaired social communication and/or interaction

and restricted and/or repetitive behaviors (American Psychological Association, 2013). As of

2014, the Centers for Disease Control and Prevention estimate that autism affects 1 in 68

children (CDC, 2014).


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Along with the changes in the definition and diagnosis of autism and an increased

prevalence of autism, autism research and advocacy groups have also increased. The

Organization for Autism Research was created in 2001 by parents and grandparents of autistic

children who believed that applied research could help answer many of the questions they

encountered in their daily lives (Research Autism, 2001). Later in 2003, the National Autism

Association, another parent run organization, formed to focus on issues related to severe autism

such as safety and crisis prevention by providing family support (National Autism Association,

2015). Another organization also formed in 2005 when Autism Speaks was founded by Bob &

Suzanne Wright to fund research, increase awareness, and advocate for autistic individuals and

their families (Autism Speaks, 2013).


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References

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disorders (1st ed.). Washington, DC: American Psychiatric Association.

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(3rd ed., text rev.). Washington, DC: Author.

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders

(5th ed.). Washington, DC: Author.

Asperger, H., & Frith, U. (1991). 'Autistic psychopathy' in childhood. In U. Frith, U. Frith

(Eds.) , Autism and Asperger syndrome (pp. 37-92). New York, NY, US: Cambridge

University Press. doi:10.1017/CBO9780511526770.002

Baio, J. (2012). Prevalence of Autism Spectrum Disorders — Autism and Developmental

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Baker, J. (2013). Autism at 70 - from Kanner to DSM-5. The New England Journal of Medicine.

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Edelson, S. (2014). “Infantile autism:” 50 years later. Autism Research Institute.

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about-naa/

Gernsbacher, M. A., Dawson, M., & Goldsmith, H. H. (2005). Three Reasons Not to Believe in
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refutation, retraction, and fraud. Indian Journal of Psychiatry, 53(2), 95–96. doi

10.4103/0019-5545.82529

Timeline: Thimerosal in vaccines (1999-2010), (2014). Centers for Disease Control and

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pervasive developmental disorder in children. The Lancet. 351, 637 – 641.

Wolff, S. (2004). The history of autism. European Child Adolescent Psychiatry. DOI 10.1007

s00787-004-0363-5

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